ライフサイエンスコーパス: microsatellite stable

1 rosatellite unstable) or non-Lynch syndrome (microsatellite stable).

2 All of the other tumors were considered microsatellite stable.

3 All 41 HER2 amplified CRCs were microsatellite stable.

4 jority are checkpoint blockade-resistant and microsatellite stable.

5 et dispensable in models of cancers that are microsatellite stable.

6 tely differentiated invasive adenocarcinoma, microsatellite stable.

7 d in the context of biallelic mutations were microsatellite stable.

8 stage II, CRC tumors, 582 of them confirmed microsatellite stable.

9 , in all cases the matched breast cancer was microsatellite stable.

10 All 13 FGPs were microsatellite stable.

11 s classified as MSI-H, MSI-indeterminate, or microsatellite-stable.

12 Of the 209 cases, 65% cancers were microsatellite stable, 21% were MSI-low, and 14% were MS

13 ctal cancers were divided into 4 groups: (1) microsatellite stable, Amsterdam-positive (MSS HNPCC) (N

14 le) of mutated genes was 5 (3-7), 5 (3-6) in microsatellite stable and 12.5 (4.5-32) in microsatellit

15 t colorectal (and other) cancers, and having microsatellite stable and unstable tumors were included.

16 ibrotic colorectal cancers (CRC) are largely microsatellite-stable and display desmoplastic stroma wi

17 Tumors were microsatellite-stable, and the median mutational burden

18 The remaining 80% to 85% of CRCs are microsatellite stable but most are characterized by chro

19 tion, the tumors from mutation carriers were microsatellite stable but tended to acquire base substit

20 and 43% of MSI colon cancers, but only 7% of microsatellite stable cancers.

21 re the best discriminators between MSI-H and microsatellite-stable cancers (odds ratio: 37.8, 9.8, an

22 Retention of 18q alleles in microsatellite-stable cancers and mutation of the gene f

23 We also found that 37.8% of microsatellite-stable cancers had no LOH events identifi

24 In microsatellite-stable cases, tumors from Nigerian patien

25 rden and signatures were observed in the 802 microsatellite-stable cases.

26 le cell lines and constitutive expression in microsatellite-stable cell lines.

27 NonRER (microsatellite stable) cell lines typically displayed hi

28 e resistant to 5-FU in culture compared with microsatellite stable cells, despite similar amounts of

29 that would allow high-resolution mapping on microsatellite-stable cells or tissues with RETrace.

30 d to WRN degradation in MSI cells but not in microsatellite-stable cells.

31 d cell death in MSI-high (MSI-H), but not in microsatellite-stable, cells.

32 esenchymal phenotype and invasiveness of the microsatellite-stable CoLo741 cells (which express endog

33 efficacy against microsatellite instable and microsatellite stable colon cancer cells.

34 cessfully generated anti-tumor immunity in a microsatellite stable colon cancer model, stimulated T-c

35 d methylator phenotype (CIMP), especially in microsatellite stable colon cancer, is not accepted univ

36 red with combination immunotherapy to battle microsatellite stable colon cancer.

37 ng for solid tumors, particularly for "cold" microsatellite stable colon cancers.

38 as acquired somatic mutations in a set of 30 microsatellite stable colon tumors.

39 We conclude that the BRAF V600E mutation in microsatellite-stable colon cancer is associated with a

40 osomal protein can predispose individuals to microsatellite-stable colon cancer.

41 ed biopsies of metastases from patients with microsatellite stable colorectal and pancreatic cancer.

42 better patient survival rates compared with microsatellite stable colorectal cancer.

43 In S2, patients with microsatellite stable colorectal carcinoma (MSS-CRC) giv

44 nt inhibitors (ICIs) are ineffective against microsatellite-stable colorectal cancer (CRC), which is

45 Several patients with microsatellite-stable colorectal cancer (MSS-CRC) had im

46 Microsatellite-stable colorectal cancer (MSS-CRC) is hig

47 me 20q amplification occurs predominately in microsatellite-stable colorectal cancer and defines a di

48 he rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tum

49 In the majority of microsatellite-stable colorectal cancers (CRCs), an init

50 of patient-derived tumoroids from seven CIN, microsatellite-stable colorectal cancers (CRCs), and one

51 anoma as well as low tumor mutational burden microsatellite-stable colorectal carcinoma samples, we d

52 antibodies significantly inhibits growth of microsatellite stable CRC by suppressing immunosuppressi

53 lopment, define four new common subgroups of microsatellite-stable CRC based on genomic features and

54 her proportion of susceptibility to sporadic microsatellite-stable CRC than previously assumed.

55 We established a human-like mouse model of microsatellite-stable CRC that undergoes metastatic rela

56 r, respectively, in adenomas associated with microsatellite-stable CRC versus microsatellite-unstable

57 ression different from those associated with microsatellite-stable CRC, and demonstrate that p12(DOC-

58 f DNA mutational instability as hallmarks of microsatellite-stable CRC.

59 netic, and epigenetic features distinct from microsatellite-stable CRC.

60 ems to be stronger than that between BMI and microsatellite-stable CRC.

61 ffer significantly from those observed among microsatellite-stable CRC.

62 (mut-) and APC mutation-positive (APC(mut+)) microsatellite stable CRCs.

63 the recently described group of hypermutant, microsatellite-stable CRCs is likely to be caused by som

64 permutant tumours and occur in about half of microsatellite-stable CRCs, often in the form of HLA cop

65 Microsatellite-stable disease was present in 110 patient

66 S phase and decreased apoptosis compared to microsatellite-stable (DOC-1+) cell lines.

67 a response against neoantigens expressed in microsatellite-stable gastrointestinal (GI) cancers, and

68 less robust, persists in the MMR-proficient/microsatellite stable group (n = 1757; HR 0.74, 95% CI 0

69 that 8-oxoG levels were elevated in several microsatellite stable human colorectal cancer cell lines

70 f immune infiltration identified a subset of microsatellite-stable immune hot tumors with increased r

71 with colon cancer diagnosed at stage II and microsatellite stable, median age 67, 30% women) and rep

72 Microsatellite stable metastatic colorectal cancer (MSS

73 Microsatellite-stable metastatic colorectal cancer is ty

74 s of immune inflammation, such as those with microsatellite-stable metastatic colorectal cancer.

75 carried a low tumor mutational burden, were microsatellite stable, mismatch repair proficient, did n

76 f sporadic CRCs and underlie a hypermutator, microsatellite-stable molecular phenotype.

77 MSI, defined as MSI high (MSI-H) or MSI-low/microsatellite stable (MSI-L/MSS), was assessed in tumor

78 satellite instability (MSI-positive) and 107 microsatellite stable (MSI-negative) tumors.

79 n with colorectal cancer risk for cases with microsatellite stable/MSI-low, CIMP-negative, BRAF-wildt

80 S1 in colorectal carcinogenesis, we selected microsatellite stable (MSS) and KRAS mutant or KRAS wild

81 The distinction between microsatellite stable (MSS) and low frequency MSI (MSI-L

82 modestly improve survival for patients with microsatellite stable (MSS) BRAF(V600E) metastatic color

83 icrosatellite instability and those that are microsatellite stable (MSS) but chromosomally unstable.

84 istinct gene expression profiles for MSI and microsatellite stable (MSS) cancers, which suggest that

85 nt clinical characteristics when compared to microsatellite stable (MSS) cancers.

86 compared with both wild-type cell lines and microsatellite stable (MSS) cell lines.

87 otility, and invasion consistent with EMT in microsatellite stable (MSS) colon cancer cells, whereas

88 Among microsatellite stable (MSS) colon cancers, we now find t

89 ively impairs the viability of MSI-H but not microsatellite stable (MSS) colorectal and endometrial c

90 D-1 blockade does not work for patients with microsatellite stable (MSS) colorectal cancer.

91 T genotype were more likely to have MSI than microsatellite stable (MSS) CRC [odds ratio (OR) 1.90; 9

92 the potential role of mutator phenotypes in microsatellite stable (MSS) CRC carcinogenesis.

93 microsatellite instability (MSI), but not in microsatellite stable (MSS) CRC cell lines and tumors.

94 microsatellite instability (MSI-H) CRCs and microsatellite stable (MSS) CRC demonstrate similar path

95 sitive to alpha-PD-1 treatment in a model of microsatellite stable (MSS) CRC.

96 comparing the transcriptional landscapes of microsatellite stable (MSS) CRCs with or without nuclear

97 and 41.3%, respectively, whereas and in the microsatellite stable (MSS) group, these were detected i

98 and the best diagnostic approaches to detect microsatellite stable (MSS) HNPCC tumors are unclear.

99 combinations with activity in patients with microsatellite stable (MSS) metastatic colorectal cancer

100 Microsatellite stable (MSS) metastatic colorectal cancer

101 However, it remains unclear whether microsatellite stable (MSS) patients with colorectal can

102 c cancer, allowing the identification, among microsatellite stable (MSS) patients, of a subset of MSI

103 m 283 patients with CRC, comparing MSI-H and microsatellite stable (MSS) patients.

104 we show that human CRC liver metastases and microsatellite stable (MSS) primary CRC have a similar p

105 Finally, a combined analysis combining all microsatellite stable (MSS) samples demonstrated a clear

106 SMAD4 loss promotes microsatellite stable (MSS) serrated tumors in an oncoge

107 nstability (CIN) is a major driving force of microsatellite stable (MSS) sporadic CRC.

108 aimed to characterise molecular features of microsatellite stable (MSS) TMB-H gastrointestinal tumou

109 robability of receiving ICIs than those with microsatellite stable (MSS) tumors (odds ratio [OR], 22.

110 All 54 MSI-H colon cancers and 20 random microsatellite stable (MSS) tumors from a population-bas

111 stability (MSI-H) sporadic CRCs, its role in microsatellite stable (MSS) tumors is debated.

112 However, microsatellite stable (MSS) tumors, are intrinsically re

113 ts reveals 24 significantly mutated genes in microsatellite stable (MSS) tumours and 16 in microsatel

114 Of these, 680 were microsatellite stable (MSS), 27 were MSI-H, and 111 were

115 Mesenchymal colorectal cancer (mCRC) is microsatellite stable (MSS), highly desmoplastic, with C

116 C, three tumor phenotypes have been defined: microsatellite stable (MSS), low-frequency MSI, and high

117 colorectal tumors and characterized them as microsatellite stable (MSS), MSI high or MSI low, CIMP h

118 Most cases of colorectal cancers (CRCs) are microsatellite stable (MSS), which frequently demonstrat

119 chromosomal instability (CIN); herein termed microsatellite stable (MSS).

120 of those that were not infected with EBV and microsatellite stable (MSS).

121 In the subgroups of MSI-H and microsatellite stable (MSS)/low-frequency MSI (MSI-L) tu

122 se ipilimumab and nivolumab in patients with microsatellite-stable (MSS) and O(6)-methylguanine-DNA m

123 the Werner syndrome helicase (WRN), whereas microsatellite-stable (MSS) cancer cells are not.

124 osatellite instability (MSI) and differ from microsatellite-stable (MSS) colorectal cancers in both p

125 , sporadic microsatellite-unstable (MSI) and microsatellite-stable (MSS) CRC patients, and cancer-fre

126 t inhibitors (ICIs) have limited activity in microsatellite-stable (MSS) or mismatch repair-proficien

127 henotypes (GMPs) underlying MSI-H, MSI-L, or microsatellite-stable (MSS) tumors have never been evalu

128 rates and survival outcomes in patients with microsatellite-stable (MSS) tumors.

129 te unstable (MSI-H) cancers and one-third of microsatellite-stable (MSS) tumors.

130 le (MSI) tumors, as well as in a subgroup of microsatellite-stable (MSS) tumors.

131 trial cancer based on microsatellite status (microsatellite-stable (MSS) vs. microsatellite-instable

132 tation, negative for KRAS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, p

133 nstability (MSI) and chromosome instability (microsatellite stable; MSS), are best understood in the

134 Microsatellite-stable, near-diploid (MSI-CIN-) colorecta

135 tric tumorigenesis, including both MSI-H and microsatellite-stable neoplasms.

136 h factor receptor therapy is recommended for microsatellite stable or proficient mismatch repair left

137 agnetic resonance imaging, for patients with microsatellite stable or proficient mismatch repair loca

138 ial growth factor therapy is recommended for microsatellite stable or proficient mismatch repair RAS

139 , including in basal-like breast cancer, and microsatellite-stable or KRAS-mutant colon cancer.

140 CHEK1 inhibition have synergistic effects in microsatellite-stable or KRAS-TP53 double-mutant colon c

141 vant therapy compared with patients who have microsatellite-stable or proficient mismatch repair (pMM

142 ethylation existed in sporadic CRCs (MSI and microsatellite stable) or normal colonic tissues.

143 response rate (24.3% in all patients; 25% in microsatellite stable patients) and durability that were

144 The genomic anomaly frequencies observed in microsatellite stable PDX reproduce those detected in no

145 In advanced ACC that is microsatellite stable, pembrolizumab provided clinically

146 b was seen in the mismatch repair-proficient/microsatellite stable population (HR = 0.79, 95% CI 0.60

147 n an MSI-H/dMMR xenograft model but not in a microsatellite stable/proficient MMR model.

148 cy in treatment of several solid tumors, but microsatellite-stable rectal cancer is largely resistant

149 %) of MSI CRC cell lines, but in none of the microsatellite stable samples (0/12).

150 hod, are an independent prognostic factor in microsatellite stable stage II CRC.

151 Among patients with microsatellite-stable stage III cancer, five-year overal

152 R, 0.55 [95% CI, 0.37 to 0.83]; P = .004) or microsatellite stable status (HR, 0.52 [95% CI, 0.32 to

153 mained significant in the proficient-MMR and microsatellite stable subgroup.

154 but no such correlations were found for the microsatellite stable subtype or late stage colorectal c

155 All POLE EDM tumours were microsatellite stable, suggesting that defects in either

156 All four tumors were microsatellite stable; three had IHC staining patterns c

157 men, 35 women; median age, 63 years); 71 had microsatellite stable tumors (MSS), 3 microsatellite ins

158 s associated with KRAS mutation (P = 0.033), microsatellite stable tumors (P = 0.015), decreased expr

159 patients with colorectal cancer (>85%) have microsatellite stable tumors that do not respond.

160 In a multivariate analysis of microsatellite stable tumors, CIMP high was related sign

161 seven patients with objective responses had microsatellite stable tumors.

162 st, no frameshift mutations were found in 70 microsatellite stable tumors.

163 umors (19.1% of MSI-H versus 2.2% of MSI-low/microsatellite stable tumors; P = 0.002).

164 SI (541 [146-8063]; P < .001), and lowest in microsatellite-stable tumors (70.5 [7-1877]; P < .001).

165 and 36.2% (26.5% to 46.7%) in patients with microsatellite-stable tumors (n = 94).

166 rs, but only 8% of MSI-low tumors and 13% of microsatellite-stable tumors (P=0.0001).

167 BRAF mutation was seen in 5% (40 of 803) of microsatellite-stable tumors and 51.8% (43 of 83) of mic

168 tumors, with variations in magnitude within microsatellite-stable tumors as prominent as those disti

169 ted with shorter DFS and OS in patients with microsatellite-stable tumors but not in patients with MS

170 tern of MS indels can accurately distinguish microsatellite-stable tumors from tumors with microsatel

171 he subgroup analysis showed in patients with microsatellite-stable tumors that both KRAS (HR for DFS:

172 patients with MSI-H, MSI-indeterminate, and microsatellite-stable tumors, respectively ( P < .001).

173 In microsatellite-stable tumors, this mutation was related

174 ith Lynch syndrome, MLH1-hypermethylated, or microsatellite-stable tumors.

175 (32.8 vs 13.5; P < .001) TILs compared with microsatellite-stable tumors.

176 ifies a previously unrecognized mechanism in microsatellite-stable tumors.

177 uished MSI-H from non-MSI-H (i.e., MSI-L and microsatellite stable) tumors and was designated the MSI

178 in less than 10% of loci were classified as microsatellite stable, whereas MSI was diagnosed in case